Autoimmune thyroiditis appears spontaneously in the OS chicken and provides an appropriate model for study of the genetic controls and pathogenetic mechanisms of organ-specific autoimmune disease. On the premise that autoimmunity is triggered by the simultaneous occurence of several independent genetic abnormalities in the same animal, three hereditary aberrations in the OS flock will be explored by means of genetic crosses and cell transfers: 1. A putative immune response gene regulating responses to homologous thyroglobulin. 2. A loss of thymus-dependent suppression of self-reactive clones of lymphocytes. 3. A functional or structural defect in the thyroid gland itself. In view of the accumulating evidence of a role for persistent viral infection in autoimmune disease, other experiments are planned to ascertain viral flora of the OS flock and determine whether any of these agents might contribute to the pathogenesis of autoimmune disease.